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*USMLE* > Nephrology > Flashcards

Nephrology Flashcards

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1
Q

Membranous Glomerulopathy:

histo (light, IF, special stain, EM)

A

light micro - diffuse GBM thickening without hypercellularity

if - GRANULAR IgG/C3 deposits along GBM

SILVER stain - SPIKE + DOME pattern (spikes of gbm stick out around domes of deposits)

em - irregular SUBEPITHELIAL immune deposits (btwn gbm and podocyte)

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2
Q

Focal Segmental Glomerulosclerosis:

histo - LM, EM

A

1 nephrotic syndrome in adults

LM - sclerosis is some (focal) glomeruli in only some parts (segmental) of each affected glomerulus; see OBLITERATED CAPILLARIES with HYALIN DEP.

EM - also podocyte FUSION + EFFACEMENT

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3
Q

Membranoproliferative Glomerulonephritis: histo + causes

A

thickening of GBM with hypercellularity

assoc. with Hep B or C

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4
Q

Mixed cryoglobulinemia

Ab type, organ changes, assoc. disease

A

IgM in glomerulus > BM thickening + hypercellularity presents as membranoproliferative GNitis

nephritic syn > hematuria and RBC casts

most common in chronic Hep C

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5
Q

Minimal Change Disease

pathophys

A

1 nephrotic syndrome in kids; idiopathic or after respiratory infection, immunization or insect sting/bite

T-cell production of a GLOMERULAR PERMEABILITY FACTOR (maybe IL-13) > capillary injury with foot process fusion > loss of negative charge causes selective albuminuria

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6
Q

Chronic Kidney Disease Complications

bones? thyroid?

A

renal osteodystrophy - hyperphosphatemia and hypocalcemia > either osteopenic high-turnover via high PTH or later PTH resistance with osteomalacia

thyroid - uremia inhibits peripheral T4-T3 conversion with HYPOthyroidism

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7
Q

Most common underlying valvular pathology predisposing to infective endocarditis

A

mitral prolapse

especially with coexistent regurgitation

platelet + fibrin deposits form spontaneously on valve via disturbed flow + endocardial injury

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8
Q

histo of kidney in renal artery stenosis

A

decreased tubular epithelial size, patchy inflammation and tubulointerstitial / glomerular fibrosis

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9
Q

Acute Interstitial Nephritis: labs + histo

A

rash, fever, new drug exposure in last 1-3 wks

high creatinine, BUN, oliguria (AKI); eosinophilia + urinary eosinophils; pyuria, hematuria + WBC casts

histo = interstitial infiltrate + edema

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10
Q

Paroxysmal Nocturnal Hemoglobinuria

pathophys, s/s, main organ involved + how?

A

mutation of PIGA gene > impaired GPI anchor protein > impaired anchoring of CD55 (DAF) and CD56 (MAC inhibitory protein) > complement-mediated hemolysis

hemolytic anemia
pancytopenia
thrombosis - at atypical sites; hepatic, portal + cerebral vv.
kidney - HEMOSIDEROSIS + thrombosis > CKD

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11
Q

Minimal Change Disease

microscopy

A

light micro - normal

IF - negative for complement and IgG

EM - podocyte effacement + fusion

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12
Q

IgA Nephropathy

syndrome? microscopy?

A

nephritic syndrome (hematuria + RBC casts)

light micro - segmental glomerular hypercellularity

IF - globular IgA deposits
EM - deposits in mesangium

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13
Q

PSGN

syndrome? microscopy?

A

nephritic syndrome 2-4 wks after group A strep

LM - cellular proliferation; neutrophils in capillaries
IF - granular deposits of C3 and IgG along GBM
EM - subEPITHELIAL HUMPS (immune deposits)

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14
Q

Anti-GBM disease

syndrome? microscopy?

A

nephritic syndrome (RPGN usually)

LM - crescent formation
IF - linear C3 and IgG on GBM
EM - GBM breakage, but no deposits seen

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15
Q

Membranous Nephropathy

syndrome? associations?

A

nephrotic syndrome

viral hepatitis, solid tumors, lupus

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16
Q

AD Polycystic Kidney Disease

mutation? presentation / cyst location/#?

A

PKD-1 or PKD-2 mutation > tubular cell proliferation + fluid secretion

cysts at ANY point in nephron; <5% nephrons affected

microscopic cysts at birth enlarge over decades, compress parenchyma > atrophy + fibrosis

mostly asymptomatic; flank pain, hematuria + hypertension; end-stage kidney by age 70

liver cysts and cerebral aneurysms

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17
Q

AR Polycystic Kidney Disease

differentiation from AD?

A

bilateral flank masses at birth or during 1st year (AD occurs later)

cysts in DCT or collecting duct (AD is anywhere in nephron)

US at birth shows large kidneys + cysts are visible if > 1 cm

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18
Q

Multicystic Dysplastic Kidney

kidney appearance/abnormalities?

A

multiple cysts of varying size; absence of pelvocaliceal system

ureteral or ureteropelvic atresia

affected kidney is nonfunctional; may be bilateral > Potter sequence

abdominal US of fetus / newborn for dx

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19
Q

Potter syndrome

A

renal abnormalities in fetus (ARPKD, bilateral renal agenesis, etc.) cause oligohydramnios

results in:
pulmonary hypoplasia
Potter facies (flat nose, recessed chin, epicanthal folds, low ears)
limb defects
CV abnormalities
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20
Q

Paraneoplastic syndromes in renal cell carcinoma

A

Hypercalcemia - via parathyroid hormone-related peptide (or prostaglandin overproduction > resorption)

Erythrocytosis - ectopic EPO

(Hepatic dysfunction - unrelated to liver mets)

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21
Q

Specific risk factors for BLADDER and RENAL cancers

A

renal - smoking, obesity, hypertension; toxin exposure (HEAVY METALS, PETROLEUM)

bladder - smoking, OCCUPATIONAL EXPOSURES (rubber, plastics, aromatic amine dyes, textiles, leather) SCHISTOSOMA haematobium and CYCLOPHOSPHAMIDE

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22
Q

Kidney injury in rhabdomyolysis

mechanism? labs?

A

Heme pigment release from myoglobin degradation in glomeruli > direct cytotoxicity + vasoconstriction > ACUTE TUBULAR NECROSIS

high CK
myoglobinuria = UA pos for blood, neg for RBCs
AKI - high BUN + creatinine
high K / P / Urate, low Ca

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23
Q

Renal Cell Carcinoma

cell origin + histo? gross appearance?

A

from PROXIMAL TUBULE cells of cortex; cuboidal/polygonal cells with abundant clear cytoplasm + “chicken wire” vasculature

spherical mass; renal vein invasion common; GOLDEN-YELLOW tissue (high lipids) with NECROSIS + hemorrhage

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24
Q

Renal Cell Carcinoma

presentation + paraneoplasia? risks?

A

hematuria, flank pain + palpable mass

polycythemia (EPO) or hypercalcemia (PTHrP)

smoking, hypertension + obesity
toxins (heavy metals, petroleum)

mostly in pts 60-70

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25
Renal Oncocytoma cell origin? gross morpho?
rare COLLECTING DUCT cell tumor homogenous brown tumor with CENTRAL STELLATE SCAR visible on imaging
26
PSGN immunofluorescence: Deposition pattern + location? Molecules deposited? 
Subepithelial granular deposits deposits of IgG, IgM and C3b
27
Lupus Nephritis Mechanism? Most common histo pattern?
T3 HS rxn - deposits can be mesangial, subendothelial, and/or subepithelial Diffuse proliferative glomerulonephritis is #1 type proteinuria + RBC casts
28
Calcium Oxalate stones how to prevent? 2 ways
1. Thiazides - increase calcium reabsorption from tubular fluid 2. Urine ALKALIZATION - via POTASSIUM CITRATE (also prevents uric acid stones) (Acetazolamide also alkalinizes urine, but metabolic acidosis result > Ca and Pi mobilization from bone > actually increases Ca stone risk)
29
Stages of acute tubular necrosis
Initiation - 24-36 hrs Maintenance - 1-3 weeks Recovery - months
30
First stage of ATN timing, causes (2 categories)
24-36 hours 1. Ischemia - hemorrhage, MI, shock, sepsis 2. Cytotoxins - contrast, aminoglycosides, myoglobin
31
Second stage to ATN timing, presentation
1-3 weeks Oliguric failure - low GFR, low urine, volume overload high creat/BUN, high K, metabolic acidosis
32
Third stage of ATN timing, presentation, complications
months Gradual urine output increase > diuresis Continued tubular impairment causes ELECTROLYTE WASTING (K, Mg, P, Ca)
33
Maintenance (2nd) stage of ATN tubular function parameters (3)
``` low osmolality (<350 mOsm/kg) high sodium (> 30 mEq/l) high fractional excretion of sodium (>1%) ```
34
Water Deprivation Testing Method + Results normal pt? central DI pt? partial / complete nephrogenic DI? primary polydipsia?
pt deprived of water for 4 hours with hourly checks of serum + urine osmolality; ADH is administered after several hours normal - urine starts around 500, raises on its own, and does not raise much more after ADH central DI - urine starts around 100, doesn't raise much on its own, and raises sharply after ADH partial/complete NDI - urine starts around 100 and raises slowly to ~ <500 with little change via ADH (partial) or doesn't raise at all (complete) primary polydipsia - urine starts around 100, and raises on its own
35
Post-Obstructive Diuresis what is it? when does it happen?
kidneys act to normalize fluid volume + solute levels after urinary obstruction occurs in a patient who is catheterized after obstruction (as in BPH)
36
TTP-HUS pentad
1. fever 2. neurological sx - progressive lethargy 3. renal failure 4. anemia 5. thrombocytopenia in setting of antecedent GI illness
37
Turner syndrome internal abnormalities (not musculoskeletal) + their consequences
CV - bicuspid aorta or COARCTATION renal - HORSESHOE kidney repro - STREAK OVARY, infertility, amenorrhea
38
AR Polycystic Kidney Disease mutation?
PKHD1 gene for FIBROCYSTIN (in renal tubules + bile ducts); mutation can be spontaneous too can cause renal insufficiency, nephromegaly and hypertension if oligohydramnios occurs > Potter sequence
39
MCC of kidney stones
IDIOPATHIC HYPERCALCIURIA with NORMOCALCEMIA (regulation via PTH/Vit D maintains normal serum Ca) (thought to be via increased GI abs, mobilization, or decreased renal reabsorption)
40
How is PAH handled in the kidney?
freely filtered AND SECRETED so it estimates RPF well with the formula... [urinary PAH] x urine flow rate / [serum PAH]
41
Unilateral renal artery stenosis changes in the affected (stenotic) kidney?
Hypoperfusion-related changes... 1. CORTICAL THINNING + atrophy - diffusely 2. TUBULAR ATROPHY - also diffuse 3. GLOMERULAR CROWDING 4. JGA ENLARGEMENT - releases high levels of renin
42
Unilateral renal artery stenosis changes in the unaffected (nonstenotic) kidney?
Hypertensive nephrosclerosis... 1. INTIMAL FIBROPLASIA 2. HYALINE ARTERIOLOSCLEROSIS (In severe cases only... 3. "ONION SKINNING" - hyperplastic arteriolosclerosis 4. FIBRINOID NECROSIS)
43
Kidney stones that form in high pH (basic) urine? and low pH (acidic) urine?
Basic - CaPi and Mg-NH4-Pi (struvite) Acidic - urate and cystine
44
where do urate stones precipitate and why?
in the distal tubules and collecting ducts because PH IS LOWEST HERE and urate precipitates at low pH
45
Renal Papillary Necrosis causes (5)
1. SICKLE CELL disease/trait - obstruct small vessels 2. ANALGESIC NEPHROPATHY - nsaids > decrease PGs and constrict afferent arteriole > ischemia 3. DIABETES - neg affects vessels 4. PYELONEPHRITIS - interstitial edema compresses vessels 5. URINARY OBSTRUCTION - same
46
Renal Papillary Necrosis macro + micro appearance
Macro - gray-white or yellow necrosis of papillae; SURFACE SCARS appear as fibrous depressions Micro -
47
Renal Papillary Necrosis s/s
sloughed papillae > TISSUE FLECKS in urine DARK/BLOODY URINE ureteral obstruction > colicky FLANK PAIN (may be costovertebral too if due to pyelonephritis)
48
Horseshoe kidney increases the risk of what? 4 things
1. Obstruction - at ureteropelvic junction 2. Infection - recurrent 3. Stones 4. Tumors - Wilms in kids; renal cell in adults
49
Location of kidneys in adult (vertebral level)
T12-L3
50
What blocks the ascent of a horseshoe kidney?
Inferior mesenteric artery
51
How can FILTRATION FRACTION be calculated?
FF = GFR/RPF fraction of total plasma flow that is filtered thru glomerulus
52
SLIGHT constriction of the efferent arteriole has what effects on... RPF GFR Filtration fraction
RPF goes down GFR goes up (via increased hydrostatic pressure) Filtration fraction goes up (FF = GFR/RPF)
53
STRONG constriction of the efferent arteriole has what effects on... RPF GFR
RPF goes down GFR goes down hydrostatic pressure increases in glomerulus, BUT loss of fluid from glomerular capillaries concentrates plasma proteins and eventually RAISES PLASMA ONCOTIC PRESSURE enough to counteract the hydrostatic pressure
54
5 renal tubular defects in order from PCT to collecting duct
Fans of Bars Git Lit Syndromatically ``` Fanconi - PCT Bartter - thick ascending Gitelman - DCT Liddle - CD Syndrome of Apparent Mineralocorticoid Excess - CD ```
55
Fanconi syndrome tubule segment + what is handled improperly?
PCT generalized REABSORPTION DEFECT AAs, glucose, bicarb and phosphate are all excreted more (+ everything else absorbed in PCT)
56
Fanconi syndrome pathophysio effects (3)
1. Metabolic Acidosis - proximal RTA 2. Hypophosphatemia 3. Osteopenia
57
Fanconi syndrome 5 categories + examples
1. Hereditary - Wilson's, tyrosinemia, glycogen issues 2. Ischemia 3. Multiple myeloma 4. Drugs/toxins - cisplatin, ifosfamide, expired tetracyclines, tenofovir 5. Lead poisoning
58
Bartter syndrome tubule segment + what is reabsorbed wrong effects (3 and all are logical once you know the defect + the drug it resembles) inheritance?
TAL - affects Na/K/2Cl cotransporter 1. Metabolic ALKALOSIS, via... 2. HYPOkalemia 3. HypercalciURIA - more Ca in urine > less in blood AR inheritance looks like chronic loop diuretic use (same transporter affected)
59
Gitelman syndrome tubule segment + reabs. defect effects (4 and all BUT ONE are logical once you know the defect) inheritance?
DCT - NaCl reabsorption affected 1. Metabolic ALKALOSIS, via... 2. HYPOkalemia 3. HypocalciURIA - less Ca in urine > more in blood 4. HypoMAGNESEMIA AR inheritance looks like chronic THIAZIDE use, except for hypomagnesemia (less severe than Bartter, just as loops are more effective than thiazides)
60
Liddle syndrome tubule + absorption issue? inheritance?
AD - only of the renal tubule disorders that is AD ("Liddle is little so he has a Napoleon complex and must be dominant") GOF mutation cause INCREASED Na reabs. via the ENaC
61
Liddle syndrome effects (4)? (think of the mutation... its effects are then the OPPOSITE of what drugs?) differential? tx?
1. Metabolic ALKALOSIS 2. Hypokalemia 3. Hypertension 4. Decreased aldosterone Diff. from hyperaldosteronism by NEARLY UNDETECTABLE serum aldo levels Tx with AMILORIDE (blocks ENaC)
62
Syndrome of Apparent Mineralocorticoid Excess 2 causes + inheritance of 1
1. AR disorder of 11B-HYDROXYSTEROID DH - can not convert cortisol to inactive cortisone in cells > has some MC activity 2. Licorice consumption - glycyrrhetinic acid inhibits enzyme
63
Syndrome of Apparent Mineralocorticoid Excess effects (4 ... all very logical) tx (2)
1. Metabolic ALKALOSIS, via... 2. Hypokalemia 3. Hypertension 4. Low serum aldo 1. K-sparing diuretics 2. Corticosteroids - to decrease endogenous production of cortisol (guess you'd have to give one with low MC activity...)
64
renal complication in sickle cell disease
papillary necrosis sickling in low pO2 environment of renal medulla > micro- or macrohematuria + flank pain in SC pt
65
what complicates abdominal surgery in patients with horseshoe kidney?
anomalous origins of MULTIPLE RENAL ARTERIES to the kidney
66
cells in what TWO PARTS of the kidney are most susceptible to anoxic injury?
PCT and thick ascending limb use most ATP (and thus O2) for transport processes
67
4 causes of renal papillary necrosis
SAAD papa S - sickle cell A - acute pyelonephritis A - analgesics D - diabetes
68
Drugs commonly causing ACUTE INTERSTITIAL NEPHRITIS (4 categories and a single drug with mnemonic; plus one extra drug)
5 Ps - drugs act as haptens ``` Pee (diuretics) Pain free (analgesics) Penicillins + cePhalosporins PPIs rifamPin ``` also sulfonamides... TMP-SMX for uti
69
what might cause SECONDARY INTERSTITIAL NEPHRITIS (other conditions, infections) (5 things)
Mycoplasma + Legionella Sjogrens SLE Sarcoidosis
70
S/s of interstitial nephritis
PYURIA - primarily EOSINOPHILIC Azotemia fever, RASH, HEMATURIA, and costovert tenderness CAN be asymptomatic!
71
Other than albumin, what two important proteins can be lost in urine in NEPHROTIC SYNDROME? hint: 1) hematological, and 2) immunological consequences
1) ANTI-THROMBIN III - increased thrombin activity > hypercoagulability; may cause renal vein thrombosis (flank pain and hematuria) or VARICOCELE if left sided 2) GAMMA GLOBULINS - increases risk of infection with encapsulated bacteria
72
Main protein lost in minimal change disease
albumin only "selective albuminuria" via loss of GBM negative charge tx with steroids (kidney function usually remains normal throughout course of MCD)
73
FSGS nephrotic syndrome causes (2 categories + general pathophys)
1. assoc. with IV DRUG USE and resulting VIRUSES (HIV, hepatitis) 2. Secondary to diseases that injure glomeruli - DM, vasculitis, HTN, SICKLE podocyte injury via direct (eg, cytotoxic drugs) or indirect (eg, glomerular hyperfiltration) mechanisms
74
Clinical differences btwn FSGS and MCD (3)
FSGS has... 1. NON-selective proteinuria 2. POOR STEROID response 3. high rate of development of END-STAGE KIDNEY in 10 years
75
1st glomerular change in diabetic nephropathy
GBM thickening via NEG
76
Later glomerular change in diabetic nephropathy
Kimmelstiel-Wilson nodules round pink deposits of laminated MESANGIAL MATRIX
77
Intracapillary change in diabetic nephropathy? considering all 3 changes, what is the other name for diabetic nephropathy that describes the pathological situation?
LM shows SCLEROSIS causing OBLITERATED CAPILLARIES with HYALINE "Nodular Glomerulosclerosis" - GBM thickening first, then K-W mesangial nodules with sclerotic capillary changes (foot processes are also effaced, as in all nephrotic syndromes)
78
Membranous Glomerulopathy causes (4 categories, examples) labs
- causes: idiopathic, or... 1. infection - viral HEPATITIS b/c or SYPHILIS 2. tumors - lung, colon, breast, prostate 3. SLE - although lupus usually nephritic 4. drugs - PENICILLAMINE or NSAIDs ANTI-PLA2R antibody (highly specific + correlates to disease activity)
79
Tx and progression of membranous glomerulopathy
Tx - steroids can slow progression abt 40% progress to ES kidney in 2-20 yrs
80
Renal amyloidosis microscopy (stains + polarized light) first sign later sign
first - focal amyloid deposits in MESANGIUM later - amyloid obliterates capillaries eventually, entire architecture of glomerulus is ruined Congo red - amyloid is pink Polarized - apple green birefringence
81
5 causes/subtypes of nephrotic syndrome
1. AMYLOID NEPHROPATHY - Congo red and polarized light 2. DIABETIC NEPHROPATHY - nodular glomerulosclerosis; k-w nodules 3. MINIMAL CHANGE DISEASE - em signs only 4. FSGS - via iv drugs/viruses, or dm/htn/vasculitis, sickle 5. MEMBRANOUS NEPHROPATHY - via sle/drugs/hepatitis/syphilis/tumors
82
Most specific sign for pyelonephritis in setting of other UTI sx
white blood cell casts
83
What 2 parts of the nephron are most susceptible to hypoxic-ischemic injury?
STRAIGHT segment of proximal tubule (medulla) Thick AL of Henle loop (medulla)
84
Anion gap calculation
AG = Na - (Cl + HCO3)
85
What is a normal anion gap value?
8-12 mEq/l
86
What causes normal anion gap metabolic acidosis? acronym? (7 words)
HARDASS 1. Hyperalimentation - eating too much 2. Addison disease 3. Renal tubular acidosis 4. Diarrhea 5. Acetazolamide 6. Spironolactone 7. Saline infusion
87
What causes INCREASED anion gap metabolic acidosis? acronym? (8)
MUDPILES 1. Methanol - formic acid metabolite 2. Uremia 3. Diabetic Ketoacidosis 4. Propylene glycol 5. Iron or Isoniazid 6. Lactic acidosis 7. Ethylene glycol - oxalic acid 8. Salicylates
88
#1 early childhood renal malignancy cell / tissue type? gene / chromosome? presentation?
Nephroblastoma - Wilms tumor - embryonic glomerular structures - WT1 or WT2 suppressor LOF on chr. 11 - LARGE, palpable, UNILATERAL flank mass +/- hematuria
89
3 syndromes that include Wilms tumor
1. WAGR - aniridia, genitourinary malf., retardation 2. DENYS-DRASH - diffuse mesangial sclerosis + dysgenesis of gonads 3. BECKWITH-WIEDEMANN - macroglossia, organomegaly, "hemihyperplasia" (WT2 mut.)
90
What is WAGR complex? | it's an acronym for all the s/s!
1. Wilms tumor 2. Aniridia - no iris 3. Genitourinary malformations 4. Retardation all due to WT1 deletion
91
What is DENYS-DRASH SYNDROME? | the name hints at 2 of the 3 issues
1. Wilms tumor - via WT1 mutation 2. gonadal Dysgenesis 3. Diffuse mesangial sclerosis - early-onset nephrosis (Dysgenesis + Diffuse sclerosis in Denys-Drash)
92
What is Beckwith-Wiedemann syndrome? | the 2nd part of the name hints at 3 of the 4 issues
1. Wilms tumor - via WT2 mutation 2. Macroglossia 3. Organomegaly 4. Hemihyperplasia (think "Wide"-man with his big tongue, organs and... hemi?)
93
Cystinuria inheritance? crystal shape?
AR hexagon
94
Cystinuria defective protein? malabsorbed molecules?
high-affin, sodium-independent DIBASIC AA TRANSPORTER in pct and intestine COLA - Cystine, Ornithine, Lysine, Arginine (but all but cystine are soluble and don't form stones)
95
Cystinuria dx (2, one simple one fancy) ? tx?
high URINARY CYSTINE SODIUM CYANIDE-NITROPRUSSIDE test - cyanide added to pee > converts cystine to cysteine > nitroprusside added and reacts with -sh grp causing RED-PURPLE color = positive urinary ALKALINIZATION (eg, acetazolamide or sodium bicarb)
96
Description of myeloma casts
WAXY and LAMINATED

*USMLE* (28 decks)

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